An experimental attempt to induce
Mycobacterium intracellulare infection in white conventional mice was made by means of an airborne infection apparatus.
Mycobacterium intracellulare, TMC 1469 strain (provided by the U. S.-japan Cooperative Medical Science Program-NIAID in 1975), was grown in Dubos Tween albumin liquid medium for ten days and stored at 4°C until each airborne challenge. The exposure apparatus used was an Airborne Infection Apparatus, Model A42, TRI-R Instruments, INC (New York, U. S. A.). At each airborne challenge, the bacillary culture was diluted five fold in distilled water (ca. 1.4×10
7 v. u./m
l) to be placed in the nebulizer, and the animals were exposed for 40 minutes to a cloud of fine droplet nuclei containing the bacilli. The mice were divided in three groups and each group underwent airborne challenge respectively for single, five and fourteen times. After the airborne infection, mice were sacrificed and quantitative culture of lungs and histopathological examinations of main organs were performed at different intervals.
In the single airborne challenge group, the viable units of bacilli in 10mg of lung was 3.0×10
2immediately after the challenge, and decreased gradually to roughly one-hundredth of the count at fourteen weeks after the challenge. In the groups of five and fourteen times airborne challenges, the number of viable units were between 1.4×10-3.1×10
3 and 9.3×10
2-5.2×10
3 respectively during the experimental periods. Thus no significant increase in the number of viable units in lungs was recognized in the three groups.
The histological changes were exclusively seen in the lungs of mice which underwent five and fourteen times airborne challenges. Mononuclear cell aggregates at various sites were most frequently seen. One mouse, sacrificed at five weeks after five times challenge, showed a granulomatous lesion. Neither proliferative nor diffuse exudative lesions were revealed, and the histological changes were thought to be weaker and less significant compared with those of infection by
M. tuberculosis.
In view of these results, further endeavours would be necessary to induce experimental
Mycobacterium intracellulare disease.
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